The larynx is located in the neck and is involved in breathing, producing sound (speech), and protecting the trachea from aspiration of food and water. FIG. 1A shows a posterior view of the anatomy of a human larynx 100 and FIG. 1B shows the larynx as viewed from above, including the epiglottis 101, thyroid cartilage 102, vocal folds/ligaments 103, cricothyroid muscle 104, arytenoid cartilage 105, posterior cricoarytenoid (PCA) muscle 106, vocalis muscle 107, cricoid cartilage 108, recurrent laryngeal nerve (RLN) 109, transverse arytenoid muscle 110, oblique arytenoid muscle 111, superior laryngeal nerve 112, hyoid bone 113 (note: the hyoid bone is not usually considered part of the larynx and is included in FIGS. 1A and 1B strictly as an aid to orientation), thyrohyoid membrane 117, and thicker lower portion of elastic membrane or conus elasticus 118. FIG. 1C shows a lateral view and FIG. 1D shows a sagittal sectional view of head and neck regions showing the larynx 100 and its structures, trachea 114, esophagus 115 and pharynx 116, including cricoarytenoid joint 119, cricothyroid joint 120, and tongue 121.
The nerves and muscles of the larynx 100 abduct (open) the vocal folds 103 during the inspiration phase of breathing to allow air to enter the lungs. And the nerves and muscles of the larynx 100 adduct (close) the vocal folds 103 during the expiration phase of breathing to produce voiced sound. At rest, respiration frequency typically varies from 12 to 25 breaths per minute. So, for example, 20 breaths per minute result in a 3 second breath duration, with 1.5 sec inspiration, and 1.5 sec exhalation phase (assuming a 50/50 ratio). The breathing frequency changes depending on the physical activity.
Unilateral and bilateral injuries or ruptures of the recurrent laryngeal nerve (RLN) 109 initially result in a temporal partial paralysis of the supported muscles in the larynx (and the hypolarynx). A bilateral disruption of the RLN 109 causes a loss of the abductor function of the posterior cricoarytenoid (PCA) muscle 106 with acute asphyxia and life-threatening conditions. This serious situation usually requires surgical treatment of the bilateral vocal cord paralysis such as cordotomy or arytenoidectomy, which subsequently restrict the voice and put at risk the physiologic airway protection.
Another more recent treatment approach to RLN injuries uses a respiration implant that electrically stimulates (paces) the PCA muscle 106 during inspiration to abduct (open) the vocal folds 103. During expiration, the vocal folds 103 relax (close) to facilitate voicing. In these respiration implant systems, the patient can adjust (vary) the pacing/respiration frequency (breaths per minute) according to his or her physical state (e.g., at rest, normal walking, stairs, etc.) by manually switching the stimulation frequency of the pacer device, the assumption being that the human body may adapt to the artificial externally applied respiration frequency—within some locking-range. Thus, the patient and the respiration pacemaker can be described as free running oscillators at almost the same frequency but without phase-matching (no phase-locking). At some time, both systems will be in phase, but at other times the systems will be out of phase and thus benefit for the patient will be reduced.
Besides laryngeal pacemakers for RLN injuries, there also are respiration implant neurostimulators that electrically stimulate the hypoglossal nerve that innervates the root of the tongue for treatment of sleep apnea. These sleep apnea treatment systems use a respiration sensor that is implemented to trigger on the inhaling phase of breathing, for example, using a bioimpedance measurement or a pressure sensor in the pleural gap.